Individually optimized hemodynamic therapy reduces complications and length of stay in the intensive care unit: a prospective, randomized controlled trial.

BACKGROUND: The authors hypothesized that goal-directed hemodynamic therapy, based on the combination of functional and volumetric hemodynamic parameters, improves outcome in patients with cardiac surgery. Therefore, a therapy guided by stroke volume variation, individually optimized global end-diastolic volume index, cardiac index, and mean arterial pressure was compared with an algorithm based on mean arterial pressure and central venous pressure. METHODS: This prospective, controlled, parallel-arm, open-label trial randomized 100 coronary artery bypass grafting and/or aortic valve replacement patients to a study group (SG; n = 50) or a control group (CG; n = 50). In the SG, hemodynamic therapy was guided by stroke volume variation, optimized global end-diastolic volume index, mean arterial pressure, and cardiac index. Optimized global end-diastolic volume index was defined before and after weaning from cardiopulmonary bypass and at intensive care unit (ICU) admission. Mean arterial pressure and central venous pressure served as hemodynamic goals in the CG. Therapy was started immediately after induction of anesthesia and continued until ICU discharge criteria, serving as primary outcome parameter, were fulfilled. RESULTS: Intraoperative need for norepinephrine was decreased in the SG with a mean (±SD) of 9.0 ± 7.6 versus 14.9 ± 11.1 µg/kg (P = 0.002). Postoperative complications (SG, 40 vs. CG, 63; P = 0.004), time to reach ICU discharge criteria (SG, 15 ± 6 h; CG, 24 ± 29 h; P < 0.001), and length of ICU stay (SG, 42 ± 19 h; CG, 62 ± 58 h; P = 0.018) were reduced in the SG. CONCLUSION: Early goal-directed hemodynamic therapy based on cardiac index, stroke volume variation, and optimized global end-diastolic volume index reduces complications and length of ICU stay after cardiac surgery.

The effects of lung recruitment on the Phase III slope of volumetric capnography in morbidly obese patients.

BACKGROUND: In this study, we analyzed the effect of the alveolar recruitment strategy (ARS) and positive end-expiratory pressure (PEEP) titration on Phase III slope (S(III)) of volumetric capnography (VC) in morbidly obese patients. METHODS: Eleven anesthetized morbidly obese patients were studied. Lungs were ventilated with tidal volumes of 10 mL x kg(-1), respiratory rates of 12-14 bpm, inspiration:expiration ratio of 1:2, and FIO2 of 0.4. ARS was performed by increasing PEEP in steps of five from 0 end-expiratory pressure to 15 cm H2O. During lung recruitment, plateau pressure was limited to 50 cm H2O whereas tidal volume was increased to the ventilator's maximum value of 1400 mL, and PEEP was increased to 20 cm H2O for 2 min. Thereafter, PEEP was reduced in steps of 5 cm H2O, from 15 to 0. VC, arterial blood gases, and lung mechanics data were determined for each PEEP step. RESULTS: S(III) decreased from 0.014 +/- 0.006 to 0.005 +/- 0.005 mm Hg/mL when 0 end-expiratory pressure was compared against 15 cm H2O of PEEP after ARS (15ARS, P < 0.05). This decrement in S(III) was accompanied by increases in PaO2 (27%, P < 0.002) and compliance (32%, P < 0.001), whereas PaCO2 decreased by 8% (P < 0.038) when comparing values before and after ARS. A good prediction of the lung recruitment effect by S(III) was derived from the receiver operating characteristic curve analysis (area under the curve of 0.81, sensitivity of 0.75, and specificity of 0.74; P < 0.001). CONCLUSION: The S(III) in VC was useful to detect the optimal level of PEEP after lung recruitment in anesthetized morbidly obese patients.

Alveolar recruitment strategy and high positive end-expiratory pressure levels do not affect hemodynamics in morbidly obese intravascular volume-loaded patients.

We evaluated the effect of the alveolar recruitment strategy and high positive end-expiratory pressure (PEEP) on hemodynamics in 20 morbidly obese (body mass index 50 +/- 9 kg/m2), intravascular volume-loaded patients undergoing laparoscopic surgery. The alveolar recruitment strategy was sequentially performed with and without capnoperitoneum and consisted of an upward PEEP trial, recruitment with 50-60 cm H2O of plateau pressure for 10 breaths, and a downward PEEP trial. Recruitment and high PEEP did not cause significant disturbances in any hemodynamic variable measured by systemic and pulmonary artery catheters. Transesophageal echocardiography revealed no differences in end-diastolic areas or evidence of segmental abnormalities in wall motion.

Monitoring of whole-body hyperthermia with transesophageal echocardiography (TEE).

UNLABELLED: Hyperthermia induces tumor cell death by a spectrum of tumor tissue changes. As whole-body hyperthermia (WBH) can cause cardiovascular complications, especially when cardiotoxic cytostatic agents are administered, invasive cardiovascular monitoring during WBH is necessary. WBH requires a great deal of expenditure and bears the risk of severe toxicity. Furthermore cardiovascular stress, alterations of cardiac index and systemic vascular resistance are major problems during WBH. The purpose of this prospective study was to evaluate cardiovascular changes in patients undergoing WBH under general anesthesia using transesophageal echocardiography (TEE) with special focus on left ventricular function. METHODS: Hemodynamic parameters were measured with standard monitoring and TEE at defined time points in 20 patients (ASA III) undergoing WBH: M37 (baseline, body temperature: 37 degrees C) after induction of anesthesia, M39 during warming up (39 degrees C), M41.8 at plateau level (41.8 degrees C), M38 during cooling period (38 degrees C). RESULTS: Invasive monitoring and TEE measurements showed signs of hyperdynamic circulation with significant increase of the heart rate (73.6 +/- 13.7 min(-1) (M37), 104.6 +/- 13.0 min(-1) (M41.8)) and significant decrease of mean blood pressure (74.9 +/- 15.3 mmHg (M37), 65.3 +/- 11.2 mmHg (M41.8)). Cardiac index (CI) nearly doubled and stroke volume index (SVI) increased significantly from M37 to M41.8. Cardiac contractility, fractional area change (FAC) and ejection fraction (EF) increased. At M38 CI, SVI, FAC and EF showed a tendency to decrease compared to M41.8 but remained elevated compared to M37. CONCLUSION: Patients undergoing WBH showed typical signs of hyperdynamic circulation without impairment of left ventricle which could be monitored excellently by TEE. We recommend using TEE especially in patients with an increased cardiac risk.

Nebivolol inhibits superoxide formation by NADPH oxidase and endothelial dysfunction in angiotensin II-treated rats.

Nebivolol is a beta(1)-receptor antagonist with vasodilator and antioxidant properties. Because the vascular NADPH oxidase is an important superoxide source, we studied the effect of nebivolol on endothelial function and NADPH oxidase activity and expression in the well-characterized model of angiotensin II-induced hypertension. Angiotensin II infusion (1 mg/kg per day for 7 days) caused endothelial dysfunction in male Wistar rats and increased vascular superoxide as detected by lucigenin-derived chemiluminescence, as well as dihydroethidine staining. Vascular NADPH oxidase activity, as well as expression at the mRNA and protein level, were markedly upregulated, as well as NOS III uncoupled, as evidenced by NO synthase III inhibitor experiments and dihydroethidine staining and by markedly decreased hemoglobin-NO concentrations. Treatment with the beta-receptor blocker nebivolol but not metoprolol (10 mg/kg per day for each drug) normalized endothelial function, reduced superoxide formation, increased NO bioavailability, and inhibited upregulation of the activity and expression of the vascular NADPH oxidase, as well as membrane association of NADPH oxidase subunits (Rac1 and p67(phox)). In addition, NOS III uncoupling was prevented. In vitro treatment with nebivolol but not atenolol or metoprolol induced a dissociation of p67(phox) and Rac1, as well as an inhibition of NADPH oxidase activity assessed in heart membranes from angiotensin II-infused animals, as well as in homogenates of Nox1 and cytosolic subunit-transfected and phorbol ester-stimulated HEK293 cells. These findings indicate that nebivolol interferes with the assembly of NADPH oxidase. Thus, inhibitory effects of this beta-blocker on vascular NADPH oxidase may explain, at least in part, its beneficial effect on endothelial function in angiotensin II-induced hypertension.